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Last Minute Step 1 Facts > Chapter 10 > Flashcards

Chapter 10 Flashcards

1
Q

is hairy leukoplakia malignant or pre-malignant?

A

Hairy leukoplakia is a white, rough (‘hairy’) patch that arises on the lateral tongue. It is usually seen in immunocompromised individuals (e.g., AIDS)
and is due to EBV-induced squamous cell hyperplasia; not pre-malignant

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2
Q

what are the three major salivary gland tumors?

A
  • pleiomorphic adenoma
  • warthin tumor
  • mucoepidermoid carcinoma
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3
Q

pleiomorphic adenoma

A

BENIGN

Stromal tissue (cartilage) and epithelial tissue (glands)

Usually arises in parotid
Most common tumor of salivary gland

Mobile, painless circumscribed mass at the angle of jaw

High rate of recurrence because of irregular margins

Rarely can transform to carcinoma….but you will know because they will have facial nerve damage

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4
Q

warthin tumor

A

BENIGN

Cystic with abundant lymphocytes and germinal center

Usually arises in parotid
2nd most common tumor of salivary gland

“Warriors from Germany love smoking”

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5
Q

mucoepidermoid carcinoma

A

MALIGNANT

Mucinous cells and squamous cells

Usually arises in parotid with facial nerve involvement

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6
Q

does a mallory weiss tear go all the way through?

A

No!! Just a laceration

Longitudinal laceration of mucosa at the gastroesophageal (GE) junction

Caused by severe vomiting, usually due to alcoholism or bulimia

Presents with painful hematemesis

Risk of Boerhaave syndrome- rupture of esophagus leading to air in the
mediastinum and subcutaneous emphysema

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7
Q

what are the veins involved in esophageal varices?

A

Arise secondary to portal hypertension

  1. Distal esophageal vein normally drains into the portal vein via the left gastric vein.
  2. In portal hypertension, the left gastric vein backs up into the esophageal vein, resulting in dilation (varices).
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8
Q

most common risk factors of squamous cell carcinoma of the esophagus

A

Alcohol and tobacco

others are then
Very hot tea
Achalasia
Esophageal web (e.g., Plummer-Vinson syndrome)
Esophageal injury (e.g., lye ingestion)
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9
Q

Location of lymph node spread depends on the level of the esophagus that is
involved. Which part of the esophagus pertains to which lymph node?

A

Location of lymph node spread depends on the level of the esophagus that is
involved.

l. Upper 1/3-cervical nodes
2. Middle 1/3-mediastinal or tracheobronchial nodes
3. Lower 1/3-celiac and gastric nodes

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10
Q

what pertains to distension of stomach and blind loop of duodenum (‘double bubble’ sign)?

A

duodenal atresia

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11
Q

what are the complications of meckels?

A

Can present during the first 2 years of life with bleeding (due to heterotopic gastric mucosa), volvulus, intussusception, or obstruction (mimics appendicitis); however, most cases are asymptomatic.

Arises due to failure of the vitelline duct to involute

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12
Q

Mucosal infarction of the small bowel can occur with marked…

A

hypotension

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13
Q

what is the pathophys of celiac disease?

A

Gluten is present in wheat and grains; its most pathogenic component is gliadin.

Once absorbed, gliadin is deamidated by tissue transglutaminase (tTG).

Deamidated gliadin is presented by antigen presenting cells via MHC class II.

Helper T cells mediate tissue damage.

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14
Q

In patients with chronic refractory celiac disease, one must consider….

A

In patients with chronic refractory celiac disease, one must consider small bowel carcinoma and enteropathy-associated T cell lymphoma (EATL)

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15
Q

what will duodenal biopsy show you in celiac disease?

A

Duodenal biopsy reveals flattening of villi, hyperplasia of crypts, and increased intraepithelial lymphocytes (Fig. 10.18). Damage is most prominent in the duodenum; jejunum and ileum are less involved.

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16
Q

what is tropical sprue?

A

TROPICAL SPRUE
A. Damage to small bowel villi due to an unknown organism resulting in
malabsorption
B. Similar to celiac disease except
1. Occurs in tropical regions (e.g., Caribbean)
2. Arises after infectious diarrhea and responds to antibiotics
3. Damage is most prominent in jejunum and ileum (secondary vitamin B12 or
folate deficiency may ensue); duodenum is less commonly involved.

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17
Q

what is whipple disease?

A

Systemic tissue damage characterized by macrophages loaded with Tropheryma whippelii organisms; partially destroyed organisms are present in macrophage lysosomes (positive for PAS).

B. Classic site of involvement is the small bowel lamina propria

  1. Macrophages compress lacteals.
  2. Chylomicrons cannot be transferred from enterocytes to lymphatics.
  3. Results in fat malabsorption and steatorrhea
    C. Other common sites of involvement include synovium of joints (arthritis), cardiac valves, lymph nodes, and CNS.
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18
Q

where do carcinoid tumors typically arise?

A

Can arise anywhere along the gut; small bowel is the most common site.
1. Grows as a submucosal polyp-like nodule (Fig. 10.20)

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19
Q

what is carcinoid syndrome due to?

A

Carcinoid syndrome is characterized by bronchospasm, diarrhea, and flushing of skin; symptoms can be triggered by alcohol or emotional stress, which stimulate serotonin release from the tumor.

20
Q

UC vs Crohns location

A

UC
Begins in rectum and can extend proximally up to the cecum (involvement is continuous); remainder of the GI tract is unaffected.

Crohns
Anywhere from mouth to anus with skip lesions; terminal ileum is the most common site, rectum is least common.

21
Q

UC vs Crohns stool

A

UC
Left lower quadrant pain (rectum) with bloody diarrhea

Crohns
Right lower quadrant pain (ileum) with non-bloody diarrhea

22
Q

UC vs Crohns histological inflammation

A

UC
Crypt abscesses with neutrophils (Fig. 10.218)

Crohns
Lymphoid aggregates with granulomas (40% of cases)

23
Q

gross morphology of UC vs crohns

A

UC
Pseudopolyps; loss of haustra (‘lead pipe’ sign on imaging, Fig. 10.21C)

“ima put this pipe up into your colon girl”

  • C*rohns
  • C*obblestone mucosa (Fig. 10.22A), Creeping fat, and strictures (‘string-sign’ on imaging, Fig. 10.228)
24
Q

what are the complications of UC vs crohns?

A

Toxic megacolon and carcinoma (risk is based on extent of colonic involvement and duration of disease; generally not a concern until > 10 years of disease)

Malabsorption with nutritional deficiency, calcium oxalate nephrolithiasis, fistula formation, and carcinoma, if colonic disease is present

25
Q

associations for UC

A

Primary sclerosing Cholangitis

OR

“hoelangitis” LMAO

and p-ANCA positivity

26
Q

associations for crohns

A

Ankylosing spondylitis, sacroiliitis, migratory polyarthritis, erythema nodosum, and uveitis

27
Q

pete davidson probably got crohns because…

A

smoking increases risk for Crohn disease

28
Q

what type of diet is associated with diverticulitis?

A

low-fiber diet

Arise where the vasa recta traverse the muscularis propria (weak point in colonic wall); sigmoid colon is the most common location.

29
Q

HEREDITARY HEMORRHAGIC TELANGIECTASIA in one sentence

A

Autosomal dominant disorder resulting in thin-walled blood vessels, especially in
the mouth and GI tract (and especially around the lips) with ruptures that can presents as bleeding.

30
Q

what is the tumor marker used for colorectal CA?

A

CEA is a serum tumor marker that is useful for assessing treatment response and detecting recurrence; not useful for screening

31
Q

Your aunt had a colonoscopy and the report says she has a polyp with gland hyperplasia and a serrated appearance. is she gonna get cancer?

A

I. Hyperplastic polyps are due to hyperplasia of glands; classically show a ‘serrated’ appearance on microscopy

i. **Most common type of polyp; usually arise in the left colon (rectosigmoid)
ii. Benign, with no malignant potential

32
Q

Your aunt had a colonoscopy and the report says she has an adenomatous polyp. is she gonna get cancer?

A

Adenomatous polyps are due to neoplastic proliferation of glands (Fig. 10.25); 2nd most common type of colonic polyp
i. Benign, but premalignant; may progress to adenocarcinoma via the
adenoma-carcinoma sequence

33
Q

what are the three steps of the adenoma-carcinoma sequence?

A

Adenoma-carcinoma sequence describes the molecular progression from normal
colonic mucosa to adenomatous polyp to carcinoma.

i. APC (adenomatous polyposis coli gene) mutations (sporadic or germline)
increase risk for formation of polyp.

ii. K-ras mutation leads to formation of polyp.

iii. p53 mutation and increased expression of COX allow for progression to
carcinoma; aspirin impedes progression from adenoma to carcinoma.

34
Q

On colonoscopy, hyperplastic and adenomatous polyps look identical. Hence, all
polyps are removed and examined microscopically.
1. Greatest risk for progression from adenoma to carcinoma is…

A

related to size > 2 cm, sessile growth (more flat along the wall), and with a particular histology called villous (long projections from it) histology.

35
Q

sometimes FAP can sometimes have some associations with it…an example of this is… (2 of them)

A

Gardner syndrome is FAP with fibromatosis and osteomas.

  1. Fibromatosis is a non-neoplastic proliferation of fibroblasts; arises in retroperitoneum (desmoid) and locally destroys tissue
  2. Osteoma is a benign tumor of bone that usually arises in the skull.

Turcot syndrome is FAP with CNS tumors (medulloblastoma and glial tumors).

36
Q

what are juvenile polyps?

A

JUVENILE POLYP
A. Sporadic, hamartomatous (benign) polyp that arises in children(< 5 years)
l. Usually presents as a solitary rectal polyp that prolapses and bleeds
B. Juvenile polyposis is characterized by multiple juvenile polyps in the stomach and colon; large numbers of juvenile polyps increase the risk of progression to
carcinoma.

37
Q

what is peutz-jeghers syndrome?

A

PEUTZ-JEGHERS SYNDROME
A. Hamartomatous (benign) polyps throughout GI tract and mucocutaneous
hyperpigmentation (freckle-like spots) on lips, oral mucosa, and genital skin;
autosomal dominant disorder
B. Increased risk for colorectal, breast, and gynecologic cancer

38
Q

what are the risk factors of acute gastritis?

A

Risk factors
l. Severe burn (Curling ulcer}-Hypovolemia leads to decreased blood supply.
2. NSAIDs (decreased PGE2)
3. Heavy alcohol consumption
4. Chemotherapy
5. Increased intracranial pressure (Cushing ulcer}-Increased stimulation of vagus
nerve leads to increased acid production.
6. Shock-Multiple (stress) ulcers may be seen in ICU patients.
D. Acid damage results in superficial inflammation, erosion (loss of superficial epithelium), or ulcer (loss of mucosal layer).

39
Q

chronic autoimmune gastritis gives you an increased risk of what kind of cancer?

A

Increased risk for gastric adenocarcinoma (intestinal type)

will see lots of goblet cells in the stomach

40
Q

why does H pylori induce chronic inflammation

A

H pylori ureases and proteases along with inflammation weaken mucosal
defenses; antrum is the most common site (Fig. 10.12).

41
Q

with H pylori, there is an increased risk of what

A

increased risk for ulceration (peptic ulcer disease), gastric adenocarcinoma (intestinal type), and MALT lymphoma

triple therapy will reverse the risk of all of these!

42
Q

rupture of the duodenal ulcer may affect what blood vessels?

A

May rupture leading to bleeding from the gastroduodenal artery (anterior ulcer) or acute pancreatitis (posterior ulcer)

43
Q

gastric ulcer rupture would typically affect what blood vessel?

A

Rupture carries risk of bleeding from left gastric artery.

44
Q

Gastric adenocarcinoma (intestinal type)

A

Gastric adenocarcinoma
(intestinal type)
MALIGNANT

Proliferation of surface epithelial cells

Large, irregular ulcer with heaped up margins

“Things that cause ulcers gone bad – such bad ulcers now they are heaped up”

Risk factors: intestinal metaplasia from things like chronic autoimmune gastritis, chronic H. pylori gastritis, nitrosamines, and blood type A

Leser-Trelat sign

Acanthosis nigricans

Lesser curvature of the antrum
More common of the two

Presents late

Can spread to Virchow node

Distant mets are most commonly to the liver; however, there are some other classic sites such as Sister Mary Joseph nodule (periumbilical region)

45
Q

Gastric adenocarcinoma (diffuse type)

A

Gastric adenocarcinoma
(diffuse type)
MALIGNANT

Proliferation of surface epithelial cells

Signet ring cells that diffusely infiltrate the gastric wall → results in a stromal reaction to the cancer (desmoplasia) → results in thickening of the stomach wall (linitis plastica)

Therefore, desmoplasia leads to linitis plastica
NOT associated with chronic H. pylori, intestinal metaplasia, or nitrosamines

Rather, most cases are due to E-cadherin mutation

Leser-Trelat sign

Acanthosis nigricans
Lesser curvature of the antrum
NOT associated with chronic H. pylori, intestinal metaplasia, or nitrosamines

Presents late

Can spread to Virchow node

Distant mets are most commonly to the liver; however, there are some other classic sites such as the b/l ovaries → Kruckenburg tumor

Last Minute Step 1 Facts (16 decks)

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